| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Endocrinology, Vol 129, 1215-1220, Copyright © 1991 by Endocrine Society
ARTICLES |
TE Porter, CD Wiles and LS Frawley
Department of Anatomy and Cell Biology, Medical University of South Carolina, Charleston 29425.
The progression from nonpregnancy through late lactation is associated with an increase in the proportion of anterior pituitary cells that secrete PRL and a comparable decrease in the percentage of cells that release GH. These fluctuations result from variations in both the number of cells that release GH or PRL alone and mammosomatotropes, cells that release both hormones concurrently. However, it has not been determined whether this reciprocal shift in PRL and GH secretors during the onset of lactation is readily reversible. In the present study, anterior pituitaries from adult virgin, late lactating, or postweaning female rats (4, 6, or 8 days) were dispersed with trypsin and subsequently assayed for PRL and GH release using reverse hemolytic plaque assays. We found that separating lactating females from their pups for only 4 days induced a reciprocal shift in the proportions of GH and PRL cells back to levels found in virgin females. Simultaneous plaque assays were then performed to determine whether this post- weaning shift in the percentages of GH and PRL secretors was due to changes in the abundance of cells that secrete each hormone alone or in the proportion of mammosomatotropes. The overall changes in GH and PRL cell proportions consisted of variations only in the fraction of cells that secreted either GH or PRL alone; no differences were observed in the percentage of mammosomatotropes or in the overall abundance of acidophils. Our results demonstrate that the reciprocal shifts in the proportions of PRL- and GH-secreting cells associated with lactation are rapidly reversible. Moreover, these results are consistent with our hypothesis that PRL and GH secretors are functionally interconvertible and further suggest that this process is bidirectional.
This article has been cited by other articles:
![]() |
I. Huerta-Ocampo, H. C. Christian, N. M. Thompson, M. M. El-Kasti, and T. Wells The Intermediate Lactotroph: A Morphologically Distinct, Ghrelin-Responsive Pituitary Cell in the Dwarf (dw/dw) Rat Endocrinology, November 1, 2005; 146(11): 5012 - 5023. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. Fu, S. Nishimura, and T. E Porter Evidence that lactotrophs do not differentiate directly from somatotrophs during chick embryonic development J. Endocrinol., November 1, 2004; 183(2): 417 - 425. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. Fu and T. E. Porter Glucocorticoid Induction of Lactotrophs and Prolactin Gene Expression in Chicken Embryonic Pituitary Cells: A Delayed Response Relative to Stimulated Growth Hormone Production Endocrinology, March 1, 2004; 145(3): 1322 - 1330. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Ramesh, W.J. Kuenzel, and J.A. Proudman Increased Proliferative Activity and Programmed Cellular Death in the Turkey Hen Pituitary Gland Following Interruption of Incubation Behavior Biol Reprod, February 1, 2001; 64(2): 611 - 618. [Abstract] [Full Text] |
||||
![]() |
R. Ramesh, R. Solow, J. A. Proudman, and W. J. Kuenzel Identification of Mammosomatotrophs in the Turkey Hen Pituitary: Increased Abundance during Hyperprolactinemia Endocrinology, February 1, 1998; 139(2): 781 - 786. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. M. Chuang, B. L. West, J. D. Baxter, and F. Schaufele Activities in Pit-1 Determine Whether Receptor Interacting Protein 140 Activates or Inhibits Pit-1/Nuclear Receptor Transcriptional Synergy Mol. Endocrinol., August 1, 1997; 11(9): 1332 - 1341. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |